Relevant bibliographies by topics / Reproductive endocrine system

Academic literature on the topic 'Reproductive endocrine system'

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Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Reproductive endocrine system"

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Visentin, Lorenzo. "6 Endocrine System and Reproductive System Riddle J T E Endocrine System and Reproductive System 138PP 0-443-03939-9." Nursing Standard 4, no. 4 (October 24, 1989): 56. http://dx.doi.org/10.7748/ns.4.4.56.s82.

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Michal, Ješeta, Chmelíková Eva, Crha Igor, Sedmíková Markéta, Žáková Jana, and Ventruba Pavel. "Endocrine disruptive compounds and male reproduction." Medical Journal of Cell Biology 6, no. 4 (December 1, 2018): 131–34. http://dx.doi.org/10.2478/acb-2018-0021.

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AbstractEndocrine disruptors (EDs) are chemical substances that affect physiological processes in the organism via hormonal regulation. The EDs are present in the environment and objects of everyday use. They are often detected in food, particularly released from packaging of canned food, but also from plastic water bottles, and they are also found in cosmetics and fertilizers. They are commonly detected in children's toys, banknotes, receipts and many more objects. Permanent and long-term utilization of EDs has harmful effects on human reproductive health mainly by interference with sex hormone synthesis and mechanism of action. The endocrine disruptors show many negative effects on male reproductive system. Any change during synthesis or activity of sex hormones can cause abnormal reproduction, including developmental anomalies of the sexual system, disruption of testicular development or deterioration of sperm quality. Mainly the impact on the development of testicles in prenatal and early postnatal period can be crucial for reproductive health in males. This review provides an overview of the EDs and their possible impact on reproductive health in males with focus on sperm quality and development of testicles.
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Коrytko, О. О. "Influence of Endocrine Diseases on Reproductive System Functioning." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY, no. 7.71 (December 29, 2015): 94–98. http://dx.doi.org/10.22141/2224-0721.7.71.2015.72598.

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Kubokawa, K., Y. Tando, and S. Roy. "Evolution of the Reproductive Endocrine System in Chordates." Integrative and Comparative Biology 50, no. 1 (May 24, 2010): 53–62. http://dx.doi.org/10.1093/icb/icq047.

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Shepelska, Ninel, Mykola Prodanchuk, and Yana Kolianchuk. "Pesticides as endocrine distruptors of the reproductive system (literature review and own research)." JOURNAL OF THE NATIONAL ACADEMY OF MEDICAL SCIENCES OF UKRAINE, Issue 1; 2021 (May 26, 2021): 49–62. http://dx.doi.org/10.37621/jnamsu-2020-1-6.

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Currently, one of the main threats to human health is undoubtedly endocrine disruptors (ED), since they directly disrupt the processes of homeostasis maintenance, controlled by the endocrine system, the purpose of which is to maintain normal functions and development in a constantly changing environment. Pesticides can disrupt the physiological functioning of many endocrine axes, including the endocrine mechanisms that ensure reproductive health. It should be noted that research aimed at preventing chemically induced reproductive disorders in the human population is one of the central areas of preventive medicine, both in terms of their importance and the complexity of the tasks being solved. Analysis and generalization of the results of our own long-term studies have shown that the selective, and, therefore, the most dangerous toxicity of pesticides for the reproductive system is determined by endocrine-mediated mechanisms of etiopathogenesis. The low level of doses inducing pathological changes in reproductive function in our studies fully confirms one of the universal signs inherent in endocrine-distruptive compounds. The above examples demonstrate a wide range of possible endocrine-mediated mechanisms of reproductive toxicity of pesticides - endocrine disruptors. However, it is very important to note that low doses may be more effective in changing some endpoints compared to high (toxic) doses. Currently, several mechanisms have been identified and studied that demonstrate how hormones and ED induce non-monotonic reactions in animal cells, tissues and organs. The reproductive system, the functioning of which is ensured by a fine balancing of the action of androgens and estrogens, is one of the systems that presents a unique opportunity for modeling a non-monotonic dose dependence. All of the above indicates the extreme danger of the impact of hormonally active agents on the reproductive health of a person and his offspring. At the same time, the threat of endocrine-mediated disorders for subsequent generations can also be realized through the induction of mechanisms of development of epigenetic transgenerational effects. Taking into account the results of studies of the mechanisms of the ED destructive action, as well as their ability to induce non-monotonic dose dependence at an extremely low dose level, it should be admitted that, apparently, there is a need to revise the paradigm of methodological approaches to the regulation of pesticides with endocrine-disruptive properties. Key words: pesticides, endocrine disruptors, reproductive system
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Chedrese, P., Martina Piasek, and Michael Henson. "Cadmium as an Endocrine Disruptor in the Reproductive System." Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry 6, no. 1 (February 1, 2006): 27–35. http://dx.doi.org/10.2174/187152206775528941.

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Choi, Donchan. "The Consequences of Mutations in the Reproductive Endocrine System." Development & Reproduciton 16, no. 4 (December 2012): 235–51. http://dx.doi.org/10.12717/dr.2012.16.4.235.

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Queiroz, Erika Kaltenecker Retto de, and William Waissmann. "Occupational exposure and effects on the male reproductive system." Cadernos de Saúde Pública 22, no. 3 (March 2006): 485–93. http://dx.doi.org/10.1590/s0102-311x2006000300003.

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A significant increase in the incidence of male infertility has been described in the international literature, raising questions about its causes. Part of this effect may result from synthetic toxic substances acting on the endocrine system (endocrine disruptors), many of which are routinely used in work processes. We provide a critical review of the specialized literature on work-related chemical substances capable of causing male infertility. Pesticides such as DDT, linuron, and others, heavy metals like mercury, lead, cadmium, and copper, and substances from various industrial uses and residues such as dioxins, polychlorinated biphenyls (PCBs), ethylene dibromide (EDB), phthalates, polyvinyl chloride (PVC), and ethanol are among the main endocrine disruptors that can cause male infertility. Based on the literature, gonadal dysfunction and congenital malformation are the main alterations caused by these substances in the male reproductive system. We conclude that despite the relative lack of studies on this issue, the relevance of such risk calls for further studies as well as measures to prevent workers' exposure to the various substances.
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Koifman, Sergio, Rosalina Jorge Koifman, and Armando Meyer. "Human reproductive system disturbances and pesticide exposure in Brazil." Cadernos de Saúde Pública 18, no. 2 (April 2002): 435–45. http://dx.doi.org/10.1590/s0102-311x2002000200008.

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The observation of reproductive disturbances in humans and in the wildlife has been reported in the last decade in different countries. Exposure to different chemicals possibly acting in the endocrine system or endocrine disruptors, including pesticides, has been a hypothesis raised to explain the observed changes. This paper aimed to present results of an epidemiological ecologic study carried out to explore population data on pesticides exposure in selected Brazilian states in the eighties and human reproductive outcomes in the nineties. Pearson correlation coefficients were ascertained between available data pesticides sales in eleven states in Brazil in 1985 and selected further reproductive outcomes or their surrogates. Moderate to high correlations were observed to infertility, testis, breast, prostate and ovarian cancer mortality. Despite the restrains of ecologic studies to establish cause-effect relationships, the observed results are in agreement with evidence supporting a possible association between pesticides exposure and the analyzed reproductive outcomes.
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Rattan, Saniya, and Jodi A. Flaws. "The epigenetic impacts of endocrine disruptors on female reproduction across generations†." Biology of Reproduction 101, no. 3 (May 11, 2019): 635–44. http://dx.doi.org/10.1093/biolre/ioz081.

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AbstractHumans and animals are repeatedly exposed to endocrine disruptors, many of which are ubiquitous in the environment. Endocrine disruptors interfere with hormone action; thus, causing non-monotonic dose responses that are atypical of standard toxicant exposures. The female reproductive system is particularly susceptible to the effects of endocrine disruptors. Likewise, exposures to endocrine disruptors during developmental periods are particularly concerning because programming during development can be adversely impacted by hormone level changes. Subsequently, developing reproductive tissues can be predisposed to diseases in adulthood and these diseases can be passed down to future generations. The mechanisms of action by which endocrine disruptors cause disease transmission to future generations are thought to include epigenetic modifications. This review highlights the effects of endocrine disruptors on the female reproductive system, with an emphasis on the multi- and transgenerational epigenetic effects of these exposures.
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Dissertations / Theses on the topic "Reproductive endocrine system"

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Ferasyi, Teuku Reza. "Mathematical model of the reproductive endocrine system in male sheep." University of Western Australia. School of Animal Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0080.

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[Truncated abstract] The activity of the reproductive endocrine axis is the result of interactions among many organs and tissues, particularly the hypothalamus, pituitary gland and gonad. However, it depends on more than the communication between anatomical structures because it is also affected by genotype, internal factors (e.g., metabolic inputs) and external factors (e.g., photoperiod, socio-sexual cues, stress, nutrition). This multifactorial complexity makes it difficult to use animal experimentation to investigate the pathways and mechanisms involved. Therefore, in this study, I have turned to mathematical modelling. The general hypothesis was that, by modelling the hormonal feedback loop that links the hypothalamus, pituitary gland and gonad, I would be able to discover the critical control points in this homeostatic system. This would allow me to inform and direct research into the processes that control reproduction, including inputs from environmental factors. My studies began with the development of a model of the negative feedback loop through which testosterone controls the secretion of pulses of gonadotrophin-releasing hormone (GnRH) by the hypothalamus. The model incorporated two critical factors: testosterone concentration and a time delay in the inhibition of the activity of the GnRH 'pulse generator' by testosterone. The general assumptions were: i) there are two positive feedforward processes (GnRH pulses stimulate LH pulses, and, in turn, LH pulses stimulate testosterone secretion); ii) testosterone exerts negative feedback that reduces the frequency of GnRH pulses. The model incorporated a group of equations that represent the GnRH pulse generator, through which the inhibitory effect of testosterone acted to reduce GnRH pulse frequency. Simulations were run with various values for the time delay in feedback and, as model development progressed, the simulations were extended to include combinations of time delays and levels of sensitivity of the GnRH pulse generator to inhibition by testosterone. The output of the simulations showed clearly that a time delay in negative feedback, as well as the concentration of testosterone, can greatly affect the frequency of GnRH pulses and the shape of the GnRH secretory profile. Importantly, the effect of the time delay depends on the sensitivity of the pulse generator to testosterone. In addition, the simulations suggested two additional components that might be involved in the control of the GnRH pulse generator: i) a delay in the rate of adaptation to a change in steroid feedback; and ii) a minimum pulse interval (maximum frequency). These studies iii therefore suggest that the regulation of the activity of the GnRH pulse generator, and thus the frequency and profile of GnRH and LH pulses, requires interactions among these four components. These interactions should be tested in animal experimentation. In the next stage, I extended the model so I could test whether the feedback delay might involve the process of aromatization in which testosterone is converted to oestradiol at brain level. ... This information can be used to direct future experimental studies that will help us to understand the factors that underlie the dynamic behaviour of the hypothalamic and pituitary systems that control reproduction.
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Jones, Maren Bell. "Effects and interactions of endocrine disrupting chemicals and diet on the mouse reproductive system." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5006.

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Thesis (M.A.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on October 29, 2007) Vita. Includes bibliographical references.
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Gyllenhammar, Irina. "Endocrine Disruption in Amphibians : Developmental Effects of Ethynylestradiol and Clotrimazole on the Reproductive System." Doctoral thesis, Uppsala universitet, Ekotoxikologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9209.

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Amphibian populations are declining world-wide and one of the suggested reasons is environmental pollutants. Studies of long-term effects on the reproductive system in frogs following larval exposure to environmental pollutants are scarce. It is therefore important to develop methods to study developmental reproductive toxicity in amphibians. In this thesis the usefulness of Xenopus tropicalis (the West African clawed frog) as a model species for a test system was investigated. Effects on the reproductive system after larval exposure to the pharmaceuticals ethynylestradiol (EE2) and clotrimazole were evaluated. The susceptibility to EE2 exposure was compared between the model species and a wild species, the European common frog (Rana temporaria). Larval exposure to EE2 caused female-biased sex ratios in both examined frog species, indicating male-to-female sex-reversal. In adult Xenopus tropicalis, male frogs that were not sex-reversed had reduced fertility and decreased amount of mature spermatozoa in the seminiferous tubules. The proportion of frogs with ovaries but lacking oviducts increased with increasing EE2-concentrations. A female frog without oviducts is sterile. The development of ovaries in sex-reversed male frogs was implied to be similar to control females. The combination of a reduced number of males, due to sex-reversal, and impaired fertility could have severe effects on frog populations. Larval exposure to clotrimazole modulated aromatase activity in gonads and brain in Xenopus tropicalis. Brain aromatase activity was decreased at the time for gonadal differentiation and gonadal aromatase activity was increased at metamorphosis. The findings in this thesis indicate that reproduction in wild frogs might be impaired by estrogenic compounds in the environment. The results combined with the short generation time supports the use of Xenopus tropicalis as a model species when evaluating long term effects of endocrine disruptors on the reproductive system in amphibians.
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Patrick, Sean Mark. "Effects of in utero- lactational- and direct exposure to selected endocrine disrupting chemicals on the rat male reproductive system." Thesis, University of Pretoria, 2015. http://hdl.handle.net/2263/53038.

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Endocrine disrupting chemicals (EDCs) are ubiquitous natural or synthetic substances, present in the environment, that possess hormonal activity. EDCs have the ability to disrupt hormonally dependent processes and potentially elicit adverse health effects in both animals and humans. Possible adverse effects on fertility and reproductive parameters following acute and chronic exposure to these chemicals have been reported in the scientific literature. However, the association between exposure to EDCs present in a malaria area and impaired male reproductive health remains inconsistent. In South Africa (SA), malaria remains a public health threat and various programs are in place in an effort to prevent malaria transmission. EDCs in a malaria endemic area in the Limpopo Province, SA were identified as: (i) the organochlorine pesticide, 1,1,1- trichloro-2,2-bis(p-chlorophenyl)ethane (DDT); (ii) the persistent metabolite of DDT, 1,1- dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE); (iii) the active substance in insecticidetreated nets (ITNs) and used for indoor residual spraying (IRS), deltamethrin (DM); (iv) the anti-oxidant used in the preparation of lubricating oil additives, resins, plasticizers and found in polyvinyl chloride (PVC), para-nonylphenol (p-NP); (v) and phytoestrogens (coumestrol, genistein, zearalenone), which form part of a normal diet. The aim of the study was to investigate the effects of in utero-, lactational- and direct exposure to selected concentrations of previously studied EDCs found in the environment on male reproductive health using the rat model. The objectives were to (1) determine the impact of in utero-, lactational- and direct exposure to EDCs on malespecific endocrine sensitive endpoints (anogenital distance and gonadosomatic index), male accessory glands (prostate, seminal vesicles), epididymis and liver (2) determine the effects of EDC exposure on epididymal sperm count and testosterone levels, (3) assess and compare the testicular histology and spermatogenesis cycle using the spermatogenesis staging program STAGES and the Johnsen Scoring system, (4) determine the possible relationship between exposure to selected EDCs and the increase incidence of testicular apoptosis. We adapted the Organization for Economic Cooperation and Development (OECD) 415 reproductive toxicity protocol to include one control and three experimental groups, a longer prenatal exposure period, and several additional endpoints. Male Sprague- Dawley rats were exposed in utero- for 2 weeks, indirectly during lactation for 3 weeks and directly for 10 weeks to cottonseed oil [control - group 1; n=24]; DDT (35mg/kg) [group 2; n=11]; DDE (35mg/kg) [group 3; n=27]; and a mixture of DDT (35mg/kg), DM (0.5mg/kg), p-NP (2.5?g/kg), genistein (2.5?g/kg), coumestrol (2.5?g/kg) and zearalenone (2.5?g/kg) [group 4; n=15]. Following exposure and at 13 weeks of age, changes in organ weights, epididymal sperm counts, histological assessments, staging of the spermatogenic cycle and testicular apoptosis were assessed. Treatment effects were found for male reproductive tract development as evidenced by anogenital distance (AGD) in newborns and in liver characteristics. Compared with AGD in the control group (group 1; 17.54 +/- 0.65mm), AGD was significantly shorter in the mixture group (group 4; 15.20 +/- 0.16mm; P = 0.005), indicating possible feminization. In comparison with the control group mean liver mass (group 1; 17.36 +/- 2.16 g), was significantly higher in all three experimental groups: DDT (group 2; 21.16 +/- 1.29g; P <0.001), DDE (group 3; 20.65 +/- 5.06g; P = 0.003) and the mixture (group 4; 19.45 +/- 2.00g; P = 0.031). Since enlargement of the liver is a marker of liver toxicity, the increase in liver mass observed in this study indicates that exposure to these selected EDCs had a significant effect on the liver of male rats. Lipid droplet formation and hepatic disorganization were present in the liver of the DDT, DDE and mixture groups suggesting that the liver may be a primary target. The changes in liver function may therefore be involved in the reproductive effects observed in this study. When animals had reached adulthood at the end of the study, the effects of EDC exposures were found for a number of endpoints. Prostate mass in the control group (group 1; 0.83 +/-0.24g) was significantly higher in the DDT group (group 2; 1.02 +/- 0.19g; P = 0.018). Prostate mass was not, however, correlated with testosterone levels which were significantly higher in the DDE and mixture groups. Testicular histology revealed marked effects in all groups including dilated tubular lumens, detachment of the seminiferous epithelium, necrosis in the interstitium, disorganization of the seminiferous epithelium with few germ cells present, reduced seminiferous tubule diameter with no lumen, absent seminiferous tubules and decreased layers of germ cells. Although these changes were not seen in all tubules, treatment was associated with decreased mean seminiferous tubule diameters, decreased epithelial thickness, and smaller luminal diameters. Application of the Johnsen scoring system showed that the treatment effects manifested primarily as a Johnsen Score of 9 tubules (a Johnsen Score of 9 is defined as a seminiferous tubules with many spermatozoa present, but germinal epithelium disorganization with marked sloughing or obliteration of the lumen). Specifically, controls had, on average, 19% abnormal tubules, compared 46%, 25% and 56% in the DDT, DDE and mixture groups, respectively. Surprisingly, however, the lesions in histology did not translate into changes in epididymal sperm counts. This suggests that spermatogenesis proceeded normally in a proportion of tubules, resulting in sperm production sufficient to maintain apparently normal epididymal sperm stores. The results of this study indicate that in utero-, lactational- and direct exposure to mixture of EDCs found in a malaria area, at the levels used here, has negative impacts on normal genital development after in utero exposure and on spermatogenesis in adulthood after combined prenatal, lactational and postnatal exposure. These findings raise concerns to EDC exposures to mothers living in malaria-areas and the reproductive health of their male offspring. Significant differences were found in the endocrine-sensitive endpoints: AGD, testosterone, testicular STAGES and Johnsen score. This study shows that in utero-, lactational- and direct exposure to EDCs present in a malaria-area negatively affects male reproductive parameters in rats. These findings raise concerns to EDC-exposures to mothers living in malaria-areas and the reproductive health of their male offspring. Since this reproductive toxicology study constitutes in utero-, lactational and direct lifespan exposure to environmentally relevant concentrations of EDCs present in a currently malaria-vector control area, these results might be considered indicative of the effects following similar human exposures. Safer alternatives should be sought particularly in malaria vector-control programs where adverse reproductive health effects have been reported following chronic exposure to these potentially harmful chemicals.
Thesis (PhD)--University of Pretoria, 2015.
School of Health Systems and Public Health (SHSPH)
PhD
Unrestricted
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Berg, Cecilia. "Environmental pollutants and the reproductive system in birds : Developmental effects of estrogenic compounds." Doctoral thesis, Uppsala University, Department of Evolutionary Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-501.

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A number of environmental pollutants have been shown to mimick the action of the female sex hormone estrogen and are, therefore, suspected to be responsible for reproductive abnormalities seen in wildlife. Test systems which can be used in hazard and risk assessment of chemicals with estrogenic effects are consequently needed. In this thesis, I propose the avian egg as an in vivo test system for estrogenic compounds. I conclude that malformation of the left testis and the Müllerian ducts (MDs: embryonic oviducts) in avian embryos can be used as endpoints to examine estrogenic activity of chemicals. MD malformation is more easily determined and thereby faster to use as an endpoint than histologically observed feminization of the testis. The usefulness of MD/oviduct malformations as biomarkers for estrogenic effects in wild birds should be considered.

The environmental pollutants bisphenol A (BPA) and o,p´-DDT induced similar effects as the synthetic estrogens, ethynylestradiol and diethylstilbestrol. BPA caused MD malformations in quail embryos and ovotestis formation in chicken embryos. o,p´-DDT induced MD malformations in both quail and chicken embryos and ovotestis in chicken embryos. The flame retardant, tetrabromobisphenol A did not induce estrogen-like effects in quail or chicken embryos, but showed a relatively high embryolethality.

Embryonic exposure to estrogen caused persisting malformations of the oviduct, as well as a changed distribution pattern of the enzyme carbonic anhydrase in the shell gland of adult females. Considering the crucial role of carbonic anhydrase in shell formation, such changes could result in decreased shell quality. I propose that eggshell thinning in avian wildlife could reflect a functional malformation in the shell gland that is induced by xeno-estrogens during embryonic development, rather than being caused by exposure of the adult bird to environmental pollutants. This hypothesis opens new possibilities for studying the mechanisms behind contaminant-induced eggshell thinning in birds.

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Abuaniza, Zaroug A. M. "Effects of green, black and rooibos tea, coffee and buchu on testosterone production by mouse testicular cultures." Thesis, University of the Western Cape, 2013. http://hdl.handle.net/11394/4584.

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Magister Scientiae (Medical Bioscience) - MSc(MBS)
Modulation of the male reproductive system occurs as a result of exposure to endocrine disrupting compounds (EDCs) in different life stages. The effects of EDCs on the male reproductive system include infertility, decreased sperm count, function and morphology, abnormal development of secondary sex characteristics, reproductive function and sexual behavior, as well as decreased libido. Phytochemicals are naturally occurring, biologically active chemical compounds in plants. They are divided into different groups. Isoflavonoids and lignans, are the two major groups of phytoestrogens. Phytoestrogens of teas, coffee and buchu have many beneficial effects on body systems such as antimutagenic, antidiabetic, anti-inflammatory, antibacterial and antiviral properties. They also elicit many adverse events, for example, heavy consumption of green and black tea may cause liver damage and added unwanted effects when combined with other herbal beverages. Chronic heavy consumption of coffee is positively correlated to acute myocardial infarction and can elevate serum cholesterol levels. Rooibos tea decreases steroidogenesis by steroid secreting cell lines.This study investigated the effects of these beverages on the male reproductive system, using a minced testes method for determination of cell viability and hormone (testosterone) production. The first objective of this study was to optimize protein supplement for in vitro testosterone production using human serum albumin (HSA) and foetal bovine serum (FBS). Testicular cultures were prepared and exposed overnight to different concentrations of both sera and then incubated for 4 hours with or without luteinizing hormone (LH). The results showed that addition of protein supplements (HSA or FBS) did not have a significant effect on testosterone production. The second objective of this study was to investigate the effects of green tea, black tea, rooibos tea, coffee and buchu on cell viability of testicular cultures. Cells were treated overnight with varying concentrations of the plant extracts followed by incubation with/without LH for 4 hours. The effects of the plant beverages on cellular protein production were determined by the Bradford assay. The results showed that treatment of cells with varying concentrations of the plant extracts (with/without LH-treatment) had no significant effect on total cellular protein. The third objective of this study was to investigate the effects of black, green and rooibos teas, coffee and buchu on testosterone production by testicular cultures. The results obtained from these experiments showed that rooibos tea and buchu did not affect testosterone production in the presence or absence of LH. The results also indicated that green tea, black tea and coffee inhibited testosterone production by mouse testis cultures in the presence of LH, but not in the absence of LH. Black tea was the most potent inhibitor of testosterone synthesis by mouse testis cultures (IC50= 48 μg/ml), followed by coffee (IC50= 64 μg/ml) and green tea (IC50= 173 μg/ml). Green tea, black tea and coffee inhibited LH-stimulated testosterone synthesis, suggesting that these beverages may impair testicular steroidogenesis in mice. Thus, in spite of their acclaimed beneficial effects, consumption of these beverages in high doses raises concerns for their inhibitory effects on male reproductive function. Further in vitro and in vivo studies are warranted to determine their exact mechanisms of action on the male reproductive system in general and testicular function in particular.
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Ruhlen, Rachel L. "Diets, estrogen environment of the fetus, and development of the reproductive tract and other systems /." free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3091965.

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Masutomi, Naoya. "Evaluation of endocrine active chemicals on endocrine/reproductive systems following transplacental and lactational exposure in rats." Kyoto University, 2004. http://hdl.handle.net/2433/147783.

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Clarke, Neil. "Seasonal effects of treated sewage effluents upon the reproduction and development of European freshwater molluscs." Thesis, Brunel University, 2009. http://bura.brunel.ac.uk/handle/2438/4458.

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The most widespread evidence of environmental endocrine disruption in aquatic wildlife is from the feminising effects of oestrogenic endocrine disrupting compounds. However, very little is known of the effects of these chemicals (and others) upon freshwater molluscs found in our river and lakes. This thesis aimed at evaluating the effects of treated sewage effluent upon the reproductive and developmental cycle of a range of commonly found European freshwater gastropod molluscs. Initial mesocosm experiments were undertaken to test a range of mollusc species for their the suitability to the experimental system, and to test adult snails for their reproductive and developmental responses during spring to summer time. With suitable species chosen, P.corneus, a pulmonate species (sequential hermaphrodite), and V. Viviparus a prosobranch species (dioeious; separate sexes), full reproductive output was assessed over summertime and into autumn, along with developmental responses amongst the F1 generation of snails. My results suggest that the affects of effluent upon the reproductive and developmental cycle of P. corneus are strongly mitigated by both day length and water temperature (day length is most important with V. viviparus); results are sensitive to seasonal effects. However, at the peak of reproduction mid summer, P. corneus produced significantly more egg masses in effluent (100% effluent particularly), and more than one parameter of reproduction was affected. Egg masses were significantly smaller in effluent and contained significantly fewer eggs per mass. Further, there were indications that total reproductive output was increased (100% effluent significantly) in effluent compared to the river water control. In the prosobranch species V. viviparus results were less convincing, however, in 100% effluent a second reproductive peak occurred that was not seen in river water. Further, in both species there was a failure of certain reproductive parameters to observe the normal seasonal decline towards winter. In P. corneus there was a failure to stop producing egg masses in effluent, in V. viviparus the second reproductive peak in effluent could also threaten their survival with winter approaching. Developmental effects in the F1 generation were the subject of preliminary investigations, however, F1 V. viviparus demonstrated a higher than normal incidence of intersex (male and female developmental features) in effluent, and P. corneus appeared to have disturbed reproductive function (disturbance of both male and female reproductive function in the ovotestis). Therefore, both of these species of molluscs demonstrated that they are sensitive to the effects of effluent in mesocosm studies. However, we need to understand much more about their responses to effluent; in particular whether these effects could have repercussions for wild mollusc populations, and whether these effects could occur over more than one generation of snail threatening the survival of wild populations of molluscs.
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Grant, Gerald F. "The association between prostaglandins and the plasminogen activator/plasmin system in the porcine ovulatory process /." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69759.

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The objectives were: (1) to determine the pre-ovulatory changes in plasminogen activator (PA) and (PA) inhibitor (PAI) activities in the porcine follicle, and, (2) to determine if changes in the PA/plasmin system associated with ovulation were prostaglandin (PG)-dependent. PA activity (change in absorbance/h/mg wet tissue weight, three gilts per treatment group) was elevated in both granulosa cells (GC) and theca interna cells (TIC) prior to human chorionic gonadotropin (hCG) administration (0.582 $ pm$ 0.171 and 0.718 $ pm$ 0.221, respectively) but returned to basal levels in these two compartments (0.023 $ pm$ 0.013 and 0.052 $ pm$ 0.024, respectively) at 29 h post-hCG. PA activity remained basal thereafter in GC but increased approximately ten-fold in the TIC (0.549 $ pm$ 0.239) at the time of ovulation (three gilts at 41 h and one of three gilts at 38 h). PAI activity did not change in TIC over the pre-ovulatory period but increased in GC as ovulation approached. PAI activity in GC peaked at 38 h (being significantly different (p $<$ 0.05) to all other times except 41 h). Although indomethacin (INDO) effectively inhibited both PG synthesis (1.1 $ pm$ 0.2 vs. 9.2 $ pm$ 0.9 ng/ml in controls) and ovulation (0 vs. 27-61% in controls), elevated PA activity (0.801 and 0.349) was detected in the TIC of two out of nine INDO-treated gilts. Levels were basal (0.074 $ pm$ 0.028) in the other gilts. These inconclusive results are believed to reflect the occurrence of ovulation earlier than predicted, in as many as 40% of control gilts, and the short duration of increased PA activity at this time. In conclusion, elevated PA activity, in GC and TIC prior to ovulation induction, may play a role in follicular development. Elevated TIC PA activity may play an important role in the ovulatory process, but is probably PG-independent.
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Books on the topic "Reproductive endocrine system"

1

D, Gordon John, and Taylor Robert N. 1953-, eds. Reproductive endocrinology and infertility: Handbook for clinicians. Arlington, VA: Scrub Hill Press, 2005.

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2

M, Lakoski Joan, Perez-Polo Jose Regino, and Rassin David K, eds. Neural control of reproductive function: Proceedings of the Fifth Galveston Neuroscience Symposium held in Galveston, Texas, May 10-13, 1988. New York: Liss, 1989.

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P, Nicolopoulou-Stamati, Hens Luc 1951-, and Howard Vyvyan, eds. Endocrine disrupters: Environmental health and policies. Dordrecht: Kluwer Academic Publishers, 2001.

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International Capri Conference on Neuroendocrine and Peripheral Disorders of Female Reproductive System: Pathophysiology and Therapies. (2nd 1992). Neuroendocrinology of female reproductive function: Proceedings of 2nd International Capri Conference on Neuroendocrine and Peripheral Disorders of Female Reproductive System--Pathophysiology and Therapies, Capri, May 1992. Carnforth, Lancs, UK: Parthenon Pub. Group, 1993.

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1935-, Speroff Leon, ed. Clinical gynecologic endocrinology and infertility. 8th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2011.

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Clark, Seena D. New chemical links to cancer: Xenoestrogens and increases in breast, prostrate [sic] & reproductive system cancers : a report from the office of Senator Tom Hayden. Sacramento, CA: Senate Publications, 1994.

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R, Olson Erik, and Naugle Jennifer E, eds. Endocrine and reproductive systems. Philadelphia: Elsevier Mosby, 2006.

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G, Creatsas, Mastorakos George, and New York Academy of Sciences, eds. Women's health and disease. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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Learning about the endocrine and reproductive systems. Berkeley Heights, NJ: Enslow Publishers, 2013.

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R, Rolland, ed. Neuro-endocrinology of reproduction: Proceedings of the VIth Reinier de Graaf Symposium, Nijmegen, the Netherlands, 27-29 August 1987. Amsterdam: Excerpta Medica, 1987.

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Book chapters on the topic "Reproductive endocrine system"

1

Chedrese, Pedro J. "Introduction to the Molecular Organization of the Endocrine/Reproductive System." In Reproductive Endocrinology, 3–11. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88186-7_1.

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Lanfranco, Fabio, and Marco Alessandro Minetto. "The Male Reproductive System, Exercise, and Training: Endocrine Adaptations." In Endocrinology of Physical Activity and Sport, 121–32. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-314-5_7.

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Lanfranco, Fabio, and Marco Alessandro Minetto. "The Male Reproductive System, Exercise, and Training: Endocrine Adaptations." In Endocrinology of Physical Activity and Sport, 109–21. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33376-8_7.

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Tena-Sempere, Manuel. "The Kisspeptin System as Putative Target for Endocrine Disruption of Puberty and Reproductive Health." In Research and Perspectives in Endocrine Interactions, 23–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-22775-2_2.

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Wira, Charles R., and John B. Josimovich. "Endocrine Control of the Secretory Immune System in the Reproductive Tract of the Female." In Gynecologic Endocrinology, 651–62. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2157-6_33.

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Tometten, Mareike, Sandra Blois, and Petra C. Arck. "Nerve Growth Factor in Reproductive Biology: Link between the Immune, Endocrine and Nervous System?" In Chemical Immunology and Allergy, 135–48. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000087962.

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Kritchevsky, Janice, and François-René Bertin. "Endocrine system." In Equine Clinical Medicine, Surgery and Reproduction, 901–22. Second edition. | Boca Raton, Florida : CRC Press, [2020] |: CRC Press, 2019. http://dx.doi.org/10.1201/9780429113680-6.

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Tsai, Jason. "Reproductive, Endocrine and Nervous Systems." In Foundations of Complementary Therapies and Alternative Medicine, 172–86. London: Macmillan Education UK, 2010. http://dx.doi.org/10.1007/978-1-137-05902-4_16.

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Wira, Charles R., Jan Richardson, and Charu Kaushic. "Sex Hormone, Glucocorticoid, and Cytokine Regulation of Mucosal Immunity in the Male and Female Reproductive Tract." In Bilateral Communication Between the Endocrine and Immune Systems, 51–72. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2616-1_4.

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"The Male Reproductive System." In Endocrine and Reproductive Physiology, 195—e2. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-323-08704-9.00009-9.

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